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  • 1995-1999  (3)
  • Cell & Developmental Biology  (1)
  • Cell wall  (1)
  • Gene regulation (TCH genes)  (1)
  • Key words:Arabidopsis  (1)
  • Linkage disequilibrium  (1)
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  • 1
    ISSN: 1432-2048
    Keywords: Key words:Arabidopsis ; Calcium ; Calmodulin ; Cell wall ; Gene regulation (TCH genes) ; Xyloglucan endotransglycosylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract. Expression of the ArabidopsisTCH genes is markedly upregulated in response to a variety of environmental stimuli including the seemingly innocuous stimulus of touch. Understanding the mechanism(s) and factors that control TCH gene regulation will shed light on the signaling pathways that enable plants to respond to environmental conditions. The TCH proteins include calmodulin, calmodulin-related proteins and a xyloglucan endotransglycosylase. Expression analyses and localization of protein accumulation indicates that the potential sites of TCH protein function include expanding cells and tissues under mechanical strain. We hypothesize that at least a subset of the TCH proteins may collaborate in cell wall biogenesis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-232X
    Keywords: Key words Myotonic dystrophy ; CTG repeat ; Haplotype A ; Linkage disequilibrium ; Multistep model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The myotonic dystrophy (DM) mutation is an unstable (CTG) n repeat, present at a copy number of 5–37 repeats on normal chromosomes but amplified to 50–3000 copies on DM chromosomes. Previous findings in Caucasian populations of a DM founder chromosome raise a question about the molecular events involved in the expansion mutation. To investigate whether a founder chromosome for the DM mutation exists in the Japanese population, we genotyped families using polymorphic markers near the (CTG) n repeat region and constructed haplotypes. Six different haplotypes were found and DM alleles were always haplotype A. To find an origin of the (CTG) n repeat mutation and to investigate the mechanism of the expansion mutation in the Japanese population we have studied 90 Japanese DM families comprising 190 affected and 130 unaffected members. The results suggest that a few common ancestral mutations in both Caucasian and Japanese populations have originated by expansion of an ancestral n = 5 repeat to n = 19–37 copies. These data support multistep models of triplet repeat expansion that have been proposed for both DM and Friedreich's ataxia.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 168-176 
    ISSN: 0730-2312
    Keywords: cadherin ; catenin ; differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cadherins form a family of cell-cell adhesion proteins that are critical to normal embryonic development. Expression of the various family members is regulated in a complex pattern during embryogenesis. Both reduced and inappropriate expression of cadherins have been associated with abnormal tissue formation in embryos and tumorigenesis in mature organisms. Evidence is accumulating that signals unique to individual members of the cadherin family, as well as signals common to multiple cadherins, contribute to the differentiated phenotype of various cell types. While a complete understanding of the regulation of cadherin expression of the molecular nature of intracellular signaling downstream of cadherin adhesion is essential to an understanding of embryogenesis and tumorigenesis, our knowledge in both areas is inadequate. Clearly, elucidating the factors and conditions that regulate cadherin expression and defining the signaling pathways activated by cadherins are frontiers for future research. J. Cell. Biochem. Suppls. 30/31:168-176, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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